title: Prenatal exposure to bisphenol A at the reference dose impairs mitochondria in the heart of neonatal rats.
abstract: Bisphenol A (BPA) exposure has been reported to be epidemiologically associated with heart disease. As mitochondria play an important role in the early development of the heart and in the pathogenesis of heart disease, the current study investigated the possibility of cardiac mitochondrial injury in neonatal rat heart prenatally exposed to BPA. Pregnant Wistar rats were exposed to BPA 50 µg kg(-1)  day(-1) or corn oil 1 ml kg(-1) by oral gavage throughout gestation. Heart samples from pups on postnatal day 1 were isolated for analysis. Ultrastructure results showed mild swelling with dissociation of cristae in myocardial mitochondria of BPA-treated rats. Additionally, mitochondrial membrane potential and the activity of respiratory chain complex II were significantly decreased. However, the activities of other three complexes (CI, CIII, CIV) and cardiac histology stayed normal. The expression levels of some key regulators involved in mitochondria energy metabolism and ATP-generating pathways were downregulated. The study demonstrated for the first time that prenatal exposure to BPA at the reference dose could impair mitochondria in the hearts of neonatal rats.
authors.affiliation: Key Laboratory of Environment and Health, Ministry of Education, State Key Laboratory of Environment Health (Incubation), Key Laboratory of Environment and Health (Wuhan), Ministry of Environmental Protection, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Jiang
authors.forename: Juan
authors.initials: J
authors.lastname: Liu
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Li
authors.forename: Huailong
authors.initials: H
authors.lastname: Chang
authors.forename: Gengqi
authors.initials: G
authors.lastname: Li
authors.forename: Bing
authors.initials: B
authors.lastname: Xu
authors.forename: Xi
authors.initials: X
authors.lastname: Chen
authors.forename: Weiyong
authors.initials: W
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Xia
authors.forename: Shunqing
authors.initials: S
authors.lastname: Xu
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds / Q000008:administration & dosage*; D004305:Dose-Response Relationship, Drug; D004734:Energy Metabolism; D005260:Female; D015870:Gene Expression; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000473:pathology; D010636:Phenols / Q000008:administration & dosage*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000503:physiopathology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013385:Succinate Dehydrogenase / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D010636:Phenols; D012333:RNA, Messenger; D013385:Succinate Dehydrogenase; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: BPA; heart; mitochondria dysfunction; prenatal exposure; reference dose